The influence of an increase in intrapleural pressure and of an increase in lung volume on the rate of formation of pulmonary edema will be independently assessed in a dog model (oleic acid) of the adult respiratory distress syndrome. Pulmonary edema will be measured after ventilation at normal lung volume and pleural pressure, normal volume and high plueral pressure, high lung volume and normal pleural pressure, and high lung volume and high pleural pressure. These four situations will be created in anesthetized closed chest animals by various combinations of end expiratory pressure and positive or negative thoracic cage pressure. During increases of pleural pressure the venous return will be restored by blood transfusion to test the hypothesis that a high pleural pressure decreases the afterload of the left ventricle, thereby lowering left atrial pressure and decreasing pulmonary edema formation. Although positive end expiratory pressure is known to improve gas exchange in the presence of pulmonary edema little is known about its effect on the rate of formation of edema. This study seeks to provide data about this and particularly about the role a positive intrathoracic pressure may play by decreasing the afterload of the left ventricle. This information is directly applicable to current methods of therapy of patients with pulmonary edema from many causes.